Osmotic shockorosmotic stressisphysiologicdysfunction caused by a sudden change in thesoluteconcentration around acell,which causes a rapid change in the movement ofwateracross itscell membrane.Underhypertonicconditions - conditions of high concentrations of eithersalts,substratesor any solute in thesupernatant- water is drawn out of the cells throughosmosis.This also inhibits the transport of substrates and cofactors into the cell thus “shocking” the cell. Alternatively, underhypotonicconditions - when concentrations of solutes are low - water enters the cell in large amounts, causing it to swell and either burst or undergoapoptosis.[1]
All organisms have mechanisms to respond to osmotic shock, with sensors andsignal transductionnetworks providing information to the cell about theosmolarityof its surroundings;[2]these signals activate responses to deal with extreme conditions.[3]Cells that have a cell wall tend to be more resistant to osmotic shock because their cell wall enables them to maintain their shape.[4]Although single-celled organisms are more vulnerable to osmotic shock, since they are directly exposed to their environment, cells in large animals such asmammalsstill suffer these stresses under some conditions.[5]Current research also suggests that osmotic stress in cells and tissues may significantly contribute to many human diseases.[6]
Ineukaryotes,calcium acts as one of the primary regulators of osmotic stress. Intracellular calcium levels rise during hypo-osmotic and hyper-osmotic stresses.
Recovery and tolerance mechanisms
editFor hyper-osmotic stress
editCalcium plays a large role in the recovery and tolerance for both hyper and hypo-osmotic stress situations. Under hyper-osmotic stress conditions, increased levels of intracellular calcium are exhibited. This may play a crucial role in the activation ofsecond messenger pathways.[7]
One example of a calcium activated second messenger molecule is MAP Kinase Hog-1. It is activated under hyper-osmotic stress conditions[8]and is responsible for an increase in the production of glycerol within the cell succeeding osmotic stress. More specifically, it works by sending signals to the nucleus that activate genes responsible for glycerol production and uptake.[8]
For hypo-osmotic stress
editHypo-osmotic stress recovery is largely mediated by the influx and efflux of several ions and molecules. Cell recovery after hypo-osmotic stress has shown to be consistent with an influx of extracellular Calcium.[9]This influx of calcium may alter the cell's permeability.[9]
Additionally, in some organisms the efflux of amino acids associated with hypo-osmotic stress can be inhibited byphenothiazines.[9]
Hypo-osmotic stress is correlated with extracellular ATP release. ATP is used to activatepurinergic receptors.[10]These receptors regulate sodium and potassium levels on either side of the cell membrane.
Osmotic damage in humans
editSee also
edit- Osmolyte
- Myo-Inositol
- TaurineandTaurine-transporting ATPase
- Creatine
- Betaines
- Trimethylglycine– A Betaine and metabolite ofCholine
- Sorbitol
- Glycerophosphocholine
References
edit- ^Lang KS, Lang PA, Bauer C, Duranton C, Wieder T, Huber SM, Lang F (2005). "Mechanisms of suicidal erythrocyte death".Cellular Physiology and Biochemistry.15(5): 195–202.doi:10.1159/000086406.PMID15956782.
- ^Kültz D, Burg M (November 1998)."Evolution of osmotic stress signaling via MAP kinase cascades".The Journal of Experimental Biology.201(Pt 22): 3015–21.doi:10.1242/jeb.201.22.3015.PMID9787121.
- ^Kültz D (November 2007)."Osmotic stress sensing and signaling in animals".The FEBS Journal.274(22): 5781.doi:10.1111/j.1742-4658.2007.06097.x.PMID17944944.
- ^"Unique Characteristics of Prokaryotic Cells".
- ^Ho SN (January 2006). "Intracellular water homeostasis and the mammalian cellular osmotic stress response".Journal of Cellular Physiology.206(1): 9–15.doi:10.1002/jcp.20445.PMID15965902.S2CID21178769.
- ^Brocker C, Thompson DC, Vasiliou V (August 2012)."The role of hyperosmotic stress in inflammation and disease".Biomolecular Concepts.3(4): 345–364.doi:10.1515/bmc-2012-0001.PMC3438915.PMID22977648.
- ^Erickson, Geoffrey R.; Alexopoulos, Leonidas G.; Guilak, Farshid (2001)."Hyper-osmotic stress induces volume change and calcium transients in chondrocytes by transmembrane, phospholipid, and G-protein pathways".Journal of Biomechanics.34(12): 1527–1535.doi:10.1016/S0021-9290(01)00156-7.PMID11716854.
- ^abKim, Jiyoung; Oh, Junsang; Sung, Gi-Ho (2016)."MAP Kinase Hog1 Regulates Metabolic Changes Induced by Hyperosmotic Stress".Frontiers in Microbiology.7:732.doi:10.3389/fmicb.2016.00732.PMC4870262.PMID27242748.
- ^abcPierce, Sidney K.; Politis, Alexander D.; Smith, Laurens H.; Rowland, Laura M. (1988)."A ca2+ Influx in Response to Hypo-Osmotic Stress May Alter Osmolyte Permeability by a Phenothiazine-Sensitive Mechanism".Cell Calcium.9(3): 129–140.doi:10.1016/0143-4160(88)90016-4.PMID3138029.
- ^Shahidullah, M.; Mandal, A.; Beimgraben, C.; Delamere, N.A. (2012)."Hyposmotic Stress Causes ATP Release and Stimulates Na,K-ATPase Activity in Porcine Lens".Journal of Cellular Physiology.227(4): 1428–1437.doi:10.1002/jcp.22858.PMID21618533.S2CID22378117.